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S100A8 modulates mast cell function and suppresses eosinophil migration in acute asthma
Jing Zhao1, Ikuko Endoh, Kenneth Hsu
1Inflammation and Infection Research Centre, School of Medical Sciences, University of New South Wales, Sydney, Australia.
Antioxidants & Redox Signaling
|December 15, 2010
Summary
S100A8 protein protects against allergic inflammation by reducing mast cell activation and eosinophil infiltration in the lungs. Its antioxidant properties are key to this protective role in conditions like asthma.
Area of Science:
- Immunology
- Pulmonology
- Biochemistry
Background:
- S100A8 is involved in inflammatory disease pathogenesis.
- It is upregulated by Toll-like receptors and corticosteroids.
- S100A8 has antioxidant properties, scavenging oxidants from phagocytes.
Purpose of the Study:
- To investigate the protective role of S100A8 in allergic inflammation.
- To determine if S100A8 modulates mast cell activation and immune cell infiltration in asthma models.
Main Methods:
- In vitro studies using mast cells and IgE-crosslinking.
- In vivo studies using a mouse model of acute asthma.
- Assessed mast cell degranulation, cytokine production, and immune cell infiltration.
- Compared S100A8 with a non-thiol reactive mutant (Cys(41)-Ala S100A8).
Main Results:
- S100A8, but not the mutant, reduced mast cell degranulation and pro-inflammatory cytokine production (IL-6, IL-4, GM-CSF) in vitro.
- S100A8 inhibited intracellular reactive oxygen species (ROS) production, reducing downstream signaling pathways.
- In asthma models, S100A8 decreased mast cell degranulation, eosinophil chemoattractant production (IL-5, eotaxin, MCP-1), and eosinophil infiltration.
- Mucus production was reduced, potentially due to suppressed IL-6 and IL-13.
Conclusions:
- S100A8 plays a protective role in allergic inflammation.
- Its protective effects are dependent on its thiol-scavenging capacity.
- S100A8 modulates mast cell activation, eosinophil recruitment, and scavenges oxidants, offering a potential therapeutic avenue for asthma.
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